Case Report

Metabolism study in an 88-year-old woman with severe hypothermia during rewarming procedures

It is commonly accepted that below a core temperature of 288C, most patients are comatose. Studying the metabolism of a victim of severe accidental hypothermia during successful rewarming procedures, we found that the metabolism increased up to 288C followed by a plateau and then a discrete rate reduction. We believe that coma and other clinical manifestations could occur when the metab- olism starts to drop sharply below that temperature.

Currently, to our knowledge, human metabolism during rewarming procedures has not been monitored for victims of unintentional hypothermia. The common classification for the severity of hypothermia (mild, 358C-328C; moderate, 328C-288C; severe, 288C-208C; profound, 208C-148C; and deep hypothermia, b148C) is based on clinical explanations and mortality [1]. Metabolism changes could shed light on the pathophysiology of hypothermia. Adult victims have made full neurological recovery with an initial core temperature as low as 13.78C [2].

Our academic hospital is located in Brussels, Belgium, in a highly populated area with a temperate climate. However, in the winter, the temperature can drop down to -158C. Prehospital emergencies are dealt with by our accident and emergency unit‘s doctors and nurses supported by Advanced life support -trained members of the fire department. Patients are transported by ambulance to our facilities.

In winter, at 9:30 am, an 88-year-old woman was found unconscious in a field. She lived for several years in a local nursing home and had high blood pressure and dementia. The dementia explains why she left the nursing home at night, around 3:00 am, through a ground-floor window, and walked across the neighboring fields. On examination by the prehospital team, there were no signs of trauma. Her blood pressure was 100 over 60 mm Hg, heart rate was 71 beat/min, and her spontaneous respira- tory rate was 7 breaths/min. Being unconscious, with a Glasgow Coma Score of 3, she was intubated for airway-protection purposes without being mechanically ventilated and then brought to hospital. No sedative or Muscle relaxant was used for tracheal intubation.

On arrival, at 9:58 am, her core body temperature, measured by an intrarectal probe, was 23.78C. Resuscitation was performed including passive External rewarming

(ie, blankets), active central rewarming (ie, gastric and bladder lavage, warmed intravenous infusion, humidified and heated oxygen), fluid resuscitation with crystalloid solution, and potassium level adjustment. At 10:15 am, she presented 3 episodes of ventricular fibrillation responding to electrical defibrillation (6 shocks in total) while her rectal temperature was still very low at 23.68C, she did not require external cardiac massage. At that time, she was connected to a ventilator under a volume control mode with an expiratory volume of 8 L/min, a frequency of 10 per minute, and an Fio₂ of 50% and no positive end expiratory pressure. The first arterial blood gases showed the following results, not corrected for temperature: pH 7.59 (7.35-7.45), Pao₂ 195 mm Hg (85-95 mm Hg), Paco₂ 19 mm Hg (35-45 mm Hg), and a lactate of 23.0 mg/dL (b11 mg/dL). Following these results, the respiratory rate was reduced to 8 per minute, after which, Ventilator settings remained unchanged until the end of the metabolic measurements. Venous blood analysis showed potassium at 3.35 mmol/L (3.5-5 mmol/L). An electrocardiogram showed the classical Osborn J wave in all leads, a variable atrioventricular block, and a prolonged QT interval (see Fig. 1). During the following 6 hours, her temperature increased by approxi- mately 18C every hour. We started the measurement of her metabolism at 11:10 am when her temperature was 24.58C, wherein we used the deltatrac metabolic monitor (Datex- Ohmeda General Electric, Helsinki, Finland). This method of estimating energy expenditure (EE) is called indirect calorimetry. Heat production is calculated from the respira- tory exchange. Respiratory Gas exchange is determined by measuring the volume of oxygen and carbon dioxide that enters and leaves the lungs during a given period of time. The computer then calculates oxygen uptake and carbon dioxide production. Every 10th of a degree, we recorded the oxygen consumption (V_O2), the carbon dioxide production (V_CO2), and the calculated EE. The carbon dioxide partial pressure is temperature-dependent as the solubility of carbon dioxide in the plasma will be significantly increased at Low Temperature, but this is not the case for exhaled carbon dioxide, so the measurement by the deltatrac monitor is a reliable estimate of EE. Fig. 2 clearly shows a fast increase in the metabolism up to 288C where it reaches a plateau followed by a slow decrease. At rest, following the Harris-Benedict’s formula, a 60-kg, 1.60-m-tall woman has an EE of 1527.76 kcal/d.

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Fig. 1 Electrocardiogram (V4) on admission showing the typical Osborn J wave (arrow) when the rectal temperature was 23.78C.

At 1:11

pm, when her temperature was 25.68C, she

rewarming procedures, changes in rectal temperature may

opened her eyes. For sedation purposes, she was started on an infusion of 5 mg/h of midazolam. We stopped the measurements when her temperature reached 29.98C, and she was transferred to the intensive care unit. During these measurements, the patient remained hemodynamically stable and did not receive inotropic support or bicarbonates. The patient was discharged from the intensive care unit 2 days after her admission to accident and emergency and was discharged from hospital 5 days later after a Full recovery.

Can we learn anything from these bedside metabolism measurements ? Isotopic measurements and direct calorim- etry cannot be considered for acute EE measurement in a resuscitation room. Indirect calorimetry is the most accurate method of measuring energy use available for critically ill patients. Considering the respiratory and hemodynamic stability of our patient, we can assume that the body’s oxygen content remained fairly constant. Therefore, the oxygen removed from the air inspired is in proportion to its cellular uptake. One cannot assume the same for the body’s carbon dioxide content, the amount of carbon dioxide released in the lung may not be equal to the carbon dioxide produced at a cellular level. This is a well-known fact for measurements made during highly intense exercise [3]. Although in this observation, we are interested in the trend of the curve rather than the accurate value of EE. We must also mention that midazolam is known to reduce the metabolic rate significantly [4], so potentially, the increase of metabolic rate after 25.68C would have been higher. The use a rectal probe is our standard way to measure body temperature when we suspect hypothermia, it provides a good estimate of the core temperature; however, during

be delayed [5,6]. Urinary bladder temperature is likely to provide a more accurate measure of the increasing body core temperature during rewarming procedures.

The clinical cutoff between moderate and severe hypo- thermia, 288C, seems to be related to major metabolic changes shown by the EE curve in Fig. 2. The likelihood of profound alteration of the neurological status (coma) and severe cardiac arrythmias (ventricular fibrillation) could partly be explained by these modifications. This said, we know that neurological manifestations after accidental hypothermia may vary from one patient to another, but below 278C, 83% of patients are comatose [7]. A better understanding of the metabolic and physiological changes in

Fig. 2 Energy expenditure in kcal per day (value axis) during rewarming procedures (rectal temperature in degree Celsius category axis) showing a fast increase between 268C and 288C.

Case Report 986.e3

hypothermia would improve management of victims of unintentional hypothermia but would also be beneficial to patients undergoing therapeutic hypothermia.

Sebastian Matthew Spencer MD, MSc

Jean Roeseler RT, PhD Franck Verschuren MD, PhD Marc Reynaert MD, PhD Fre’de’ric Thys MD, PhD Acute Medicine Department University of Louvain

B-1200 Bruxelles, Belgium E-mail address: [email protected]

doi:10.1016/j.ajem.2007.02.033

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3. Wilmore JH, Costill DL, editors. Physiology of sport and exercise. 3rd ed. Champaign (Ill)7 Human Kinetics; 2004. p. 133 - 48.
4. Terao Y, Miura K, Saito M, et al. Quantitative analysis of the relationship between sedation and resting energy expenditure in postoperative patients. Crit Care Med 2003;31(3):830 - 3.
5. Lilly J, Boland J, Zekan S. Urinary bladder temperature monitoring: a new index of body core temperature. Crit Care Med 1980;8:742.
6. Greenes D, Fleisher G. When body temperature changes, does rectal temperature lag? J Pediatr 2004;144(6):824 - 6.
7. Fischbeck K, Simon R. Neurological manifestations of accidental hypothermia. Ann Neurol 1981;10(4):384 - 7.